Background

Yersinia pseudotuberculosis is the least common of the 3 main Yersinia species that cause infections in humans. Y pseudotuberculosis primarily causes zoonotic infection in various hosts, including domestic and sylvatic animals and birds, but has been associated with food-borne infection in humans.
[1] A few outbreaks of Y pseudotuberculosis infections in humans have been reported. In 2006, Y pseudotuberculosis was implicated in a large point-source outbreak of gastroenteritis attributed to the ingestion of raw grated carrots contaminated during the early phase of the production process. This was supported by epidemiologic, clinical, laboratory, and environmental data.
[2]

Y pseudotuberculosis infection in humans usually leads to a gastroenteritis (diarrheal component uncharacteristic) characterized by a self-limited mesenteric lymphadenitis that mimics appendicitis. Y pseudotuberculosis invades mammalian cells and survives intracellularly; the primary virulence factor is a plasmid-encoded protein that causes increased invasiveness. Postinfectious complications include erythema nodosum and reactive arthritis. Thus, a major triad for Y pseudotuberculosis infection includes fever, abdominal pain, and rash. In rare cases, it has been associated with septic complications (often in immunocompromised patients with chronic liver diseases).

The bacillus was first described in 1889 and was later renamed twice before the current name, Y pseudotuberculosis, was established in the 1960s. From the late 1920s to the mid 1960s, the organism was identified as Pasteurellapseudotuberculosis and then Shigella pseudotuberculosis. A Russian researcher named Znamenskiy demonstrated that Y pseudotuberculosis was, in fact, a causative agent for clinical illness through self-inoculation.

The genus Yersinia also contains the important species Yersinia enterocolitica and Yersinia pestis. Genomic characterization studies using hybridization techniques suggest that the selective loss of certain genes over time allowed interspecies and intraspecies diversity involving Y pseudotuberculosis and Y pestis, the organism that causes plague.
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Pathophysiology

Y pseudotuberculosis infections in humans are primarily acquired through the gastrointestinal tract after consumption of contaminated food products. Characteristic of yersinial infections, an inoculum of 109 organisms is often needed to induce infection. Although Y pseudotuberculosis infections generally do not cause diarrheal symptoms, they can cause a range of morbidities, including forms of mesenteric lymphadenitis, granulomatous disease, and dissemination with sepsis. Recent evidence has suggested that Y pseudotuberculosis may also disseminate from sites of bacterial replication within the intestinal tract and not necessarily from regional lymph nodes.
[6]

In 1959, an epidemic that occurred on the Pacific coast of Russia was termed Far East scarlet-like fever (FESLF). Y pseudotuberculosis strains associated with FESLF were recently genetically sequenced, showing mobile gene pools that contain unique plasmids, the expression of which could result in scarlatinoid fever. Interestingly, virulence factors such as the Y pseudotuberculosis –derived mitogen (YPM) — a superantigen — are likely related to the atypical scarlet fever syndromes reported more recently, such as Izumi fever in Japan. YPM includes at least 3 superantigens — YPMa, YPMb, and YPMc — all of which have pathogenetic relevance and differfrom other bacterial superantigens.

Although, as of 2007, no single infectious etiology has been shown to cause Kawasaki disease, the condition appears to be more prevalent among populations exposed to Y pseudotuberculosis infection. Kawasaki disease is found mostly in Japan (170,000 cases over 40 y); however, outbreaks of Kawasaki disease have been reported in Korea, the United States, Finland, and other non-Asian countries. Kawasaki disease and Y pseudotuberculosis infection have similar age, sexual, and temporal predilections (higher incidence in the winter months).
[7] Clinical comparisons of patients with Kawasaki disease with and without laboratory evidence of Y pseudotuberculosis infection has suggested that Y pseudotuberculosis infection may be associated with the development of coronary artery lesions and a poor treatment outcome in patients with Kawasaki disease.
[8, 9]

The incubation period of Y pseudotuberculosis infection varies from 5-10 days. Fecal excretion of the organism can occur several weeks after illness but often does not result in secondary person-to-person transmission or clinical relapses. A latent duration of 2-20 days has been reported in sporadic outbreaks, with peak incidence rates at 4 days after ingestion.

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Epidemiology

Frequency

United States

No specific pattern of Y pseudotuberculosis infection in the United States has been reported. Most Yersinia -related outbreaks in the United States and abroad have been associated with Y enterocolitica rather than Y pseudotuberculosis. In 1976, an outbreak of Y enterocolitica infection in children in Oneida, New York, was caused by contaminated chocolate milk. This was the first food-borne Yersinia -related outbreak reported in the United States, with both of the above Yersinia species being studied. Drinking from well water, mountain streams, and soil is associated with infection. Epidemics of Y pseudotuberculosis infection are uncommon, unlike the increased frequency of outbreaks associated with Y enterocolitica.

International

The distribution of Y pseudotuberculosis infection is worldwide. Most cases occur in winter, probably because of the increased seasonal incidence of infection among animals. The increased prevalence in winter may also be due to the enhanced growth characteristics in cold temperatures. Although many cases of Y pseudotuberculosis infection have been reported in Europe, large-scale outbreaks in the Aomori region of Japan were noted in the early 1990s. Fewer than 30 cases of associated septicemia have been reported in the literature.
[10]

In November 1998, 4 laboratory-confirmed cases of Y pseudotuberculosis infection were reported to the British Columbia Centre for Disease Control Society (BCCDCS).
[11] Through a follow-up case-control study evaluating risk factors in a multivariate analysis, possibly contaminated homogenized milk was implicated in the outbreak. In 1991, children consuming untreated drinking water in Okayama, Japan, were exposed to Y pseudotuberculosis, leading to clinical disease.
[12] Isolation of Y pseudotuberculosis in well water has also been reported (in Czechoslovakia). In spring 2014, an outbreak in Finland was associated with the consumption of raw milk.
[13]

In the 1980s, outbreaks of Y pseudotuberculosis infection in Finland and Japan constituted most of the sporadic cases reported in the literature. In 1995, 8 cases of Y pseudotuberculosis infection in a Belgian hospital caused gastrointestinal symptoms .
[14] The organism was isolated with stool analysis and careful isolation techniques involving cold-enriched media.

Mortality/Morbidity

Most Y pseudotuberculosis infections are self-limited with a low case-fatality rate. However, the uncommon sepsis-associated illnesses caused by Y pseudotuberculosis infection in patients with chronic liver disease may carry a mortality rate that exceeds 75%.

Race

Y pseudotuberculosis infections appear to have no specific racial or ethnic predilection.

Sex

Y pseudotuberculosis infections are 3 times more common in men than in women. However, the postinfectious complications of erythema nodosum and arthritis are more common in women.

Age

More than 75% of patients with Y pseudotuberculosis infection are aged 5-15 years.